More people die of heart disease than any other single cause. One common form of heart disease is congestive heart failure.
Congestive heart failure (CHF) is a debilitating, end-stage disease in which abnormal function of the heart leads to inadequate bloodflow to fulfill the needs of the body's tissues. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not appropriately fill with blood between heartbeats and the valves regulating blood flow may become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness, and inability to carry out daily tasks may result.
Not all CHF patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive.
As CHF progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles to grow in volume in an attempt to pump enough blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in ventricular filling.
Current standard treatment for heart failure is typically centered around medical treatment using ACE inhibitors, diuretics, and digitalis. It has also been demonstrated that aerobic exercise may improve exercise tolerance, improve quality of life, and decrease symptoms. Only an option in 1 out of 200 cases, heart transplantation is also available. Other cardiac surgery is also indicated for only a small percentage of patients with particular etiologies. Although advances in pharmacological therapy have significantly improved the survival rate and quality of life of patients, patients who are refractory to drug therapy have a poor prognosis and limited exercise tolerance. Cardiac pacing has been proposed as a new primary treatment for patients with drug-refractory CHF.
In patients with heart failure and atrial fibrillation (AF), the heart has often remodeled due to the disease, such that there is interstitial fibrosis and myocyte lengthening. There is also decreased myocyte density with increased collagenation in the connective structure of the myocardium. There is further abnormal calcium handling at both the sarcoplasmic reticulum and membrane levels. Manifestations of these effects are increased fractionation of heart electrical activity, decreased conduction velocity, and increased heterogeneity of repolarization.
Bi-chamber pacing (biventricular or biatrial) has been proposed as an emerging therapy for the treatment of heart failure and atrial fibrillation. The patients who appear to gain the greatest benefit from this pacing therapy are those with the greatest dyssynchrony, since the benefit of bi-chamber pacing appears dependent upon chamber synchronization and/or appropriate sequencing.
It is desirable to have a system, which would track the progression or regression of the patient's disease, particularly as it relates to the success of any therapy in halting or reversing the remodeling. By tracking the progression or regression of heart disease, such as CHF, more closely, treatments could be managed more effectively. Commonly, patients with heart disease have an implanted cardiac stimulation device. Hence, it would be advantageous if the implanted cardiac stimulation device were able to aid in the tracking of the progression or regression of the heart disease. The present invention provides a system and method for use in such a device capable of tracking heart disease progression or regression.